Thurston Rebecca C, Doyle Caroline Y, Kusters Cynthia D J, Chang Yuefang, Koenen Karestan, Maki Pauline, Carroll Judith E
Department of Psychiatry, University of Pittsburgh.
Cousins Center for Psychoneuroimmunology, University of California, Los Angeles.
Health Psychol. 2025 Jun 16. doi: 10.1037/hea0001523.
Trauma exposure may be linked to accelerated biological aging. However, studies have largely considered childhood abuse, with limited consideration of lifetime trauma exposure, particularly for women. Furthermore, few studies have considered newer epigenetic clocks, which have enhanced links with health outcomes. Among midlife women, we investigated whether lifetime trauma exposure is associated with older epigenetic age with several generations of clocks. We explored associations between childhood maltreatment and epigenetic age and racial differences in associations between trauma and epigenetic age.
Two hundred sixteen women ( = 59 years, 83% non-Hispanic White, 13% Black, and 4% other race/ethnicities) underwent physical measures, questionnaires to assess lifetime trauma exposure, and a blood draw. A subset of 123 women completed childhood maltreatment measures. Extrinsic epigenetic age, GrimAge, principal component-based PhenoAge, and DunedinPACE were calculated. Clocks were residualized for age and Z-scored for analysis. Associations between trauma and epigenetic age were estimated in linear regression (covariates race, education, body mass index, and estimated cell counts). Interactions by race were tested.
Relative to women without trauma exposure, those with ≥ 2 lifetime traumas had older epigenetic age, GrimAge, 1: = 0.15 (0.15), = .31, 2+: ) = 0.39 (0.13), = .004; DunedinPACE, 1: ) = 0.23 (0.12), = .07, 2+: = 0.33 (0.11), = .003. Childhood sexual abuse was also associated with older epigenetic age, GrimAge: = 0.56 (0.24), = .021. Exploratory models suggested that trauma was related to epigenetic age primarily among Black women.
Among midlife women, greater lifetime trauma and possibly childhood sexual abuse were associated with older epigenetic age, independent of chronologic age. Black women may be particularly affected. (PsycInfo Database Record (c) 2025 APA, all rights reserved).
创伤暴露可能与生物衰老加速有关。然而,以往研究大多关注童年期虐待,对终生创伤暴露的考虑有限,尤其是对女性而言。此外,很少有研究考虑更新的表观遗传时钟,而这些时钟与健康结果的联系更为紧密。在中年女性中,我们使用几代时钟研究了终生创伤暴露是否与表观遗传年龄增大有关。我们探讨了童年期虐待与表观遗传年龄之间的关联,以及创伤与表观遗传年龄关联中的种族差异。
216名女性(平均年龄 = 59岁,83%为非西班牙裔白人,13%为黑人,4%为其他种族/族裔)接受了身体测量、评估终生创伤暴露的问卷以及血液采集。123名女性的子集完成了童年期虐待测量。计算了外在表观遗传年龄、GrimAge、基于主成分的PhenoAge和达尼丁PACE。时钟针对年龄进行了残差化处理,并进行Z分数转换以进行分析。在线性回归中估计创伤与表观遗传年龄之间的关联(协变量包括种族、教育程度、体重指数和估计的细胞计数)。检验了种族间的相互作用。
与未经历创伤暴露的女性相比,经历≥2次终生创伤的女性表观遗传年龄更大,GrimAge方面,1次创伤:β = 0.15(0.15),p = 0.31,2次及以上创伤:β = 0.39(0.13),p = 0.004;达尼丁PACE方面,1次创伤:β = 0.23(0.12),p = 0.07,2次及以上创伤:β = 0.33(0.11),p = 0.003。童年期性虐待也与表观遗传年龄增大有关,GrimAge:β = 0.56(0.24),p = 0.021。探索性模型表明,创伤与表观遗传年龄的关联主要存在于黑人女性中。
在中年女性中,更多的终生创伤以及可能的童年期性虐待与更大的表观遗传年龄有关,且独立于实际年龄。黑人女性可能受影响尤为明显。(《心理学文摘数据库记录》(c)2025美国心理学会,保留所有权利)